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Modulation of T cell activation by the Beta2-Adrenergic Receptor

Beta2 肾上腺素受体对 T 细胞活化的调节

基本信息

批准号：
418522-2013
负责人：
Darlington, Peter
金额：
$ 2.33万
依托单位：
Concordia University
依托单位国家：
加拿大
项目类别：
Discovery Grants Program - Individual
财政年份：
2018
资助国家：
加拿大
起止时间：
2018-01-01 至 2019-12-31
项目状态：
已结题

来源：
https://www.nserc-crsng.gc.ca/ase-oro/Details-Detailles_eng.asp?id=648666
关键词：
Modulation cell activation Beta2 Adrenergic

项目摘要

BACKGROUND: Adaptive immune responses are coordinated by T lymphocytes, a white blood cell that circulates through blood and lymphatics of most vertebrate animals. One area that has not been widely explored is the effects of stress-activated hormones such as catecholamines, for example noradrenaline and adrenaline. T lymphocytes can sense catecholamines through a receptor called the beta2-adrenergic receptor, but how this alters adaptive immune responses is not very well understood. ****HYPOTHESIS AND RATIONALE: The hypothesis is that the catecholamines can either inhibit or activate T lymphocytes, depending on the types of signals from the beta2-adrenergic receptor. The first objective of this research program is to study in detail how the beta2-adrenergic receptor sends signals to T lymphocytes. The second objective of the program is to determine how catecholamines affect the ability of T lymphocytes to function in terms of their expansion and effector functions that are relevant to immunity. ****SIGNIFICANCE: Adaptive immune responses are necessary to fight infections, but can also cause autoimmunity, a condition where a person's own organs are attacked by the immune system. Autoimmune conditions affect millions of Canadians especially women. The link with catecholamines suggests that stress (chronic and otherwise) would affect adaptive immunity. The anticipated results we will achieve will increase our basic understanding of the immune system, and help scientists and doctors better treat infections and autoimmunity. The work also applies to maintaining healthy immunity in livestock and fish. ******

背景：适应性免疫反应由T淋巴细胞协调，T淋巴细胞是一种白细胞，在大多数脊椎动物的血液和淋巴管中循环。一个尚未被广泛研究的领域是应激激活激素的影响，例如儿茶酚胺，例如去甲肾上腺素和肾上腺素。T淋巴细胞可以通过一种名为β2-肾上腺素能受体的受体感受儿茶酚胺，但这如何改变适应性免疫反应还不是很清楚。*假设和原理：假设儿茶酚胺可以抑制或激活T淋巴细胞，这取决于来自β2肾上腺素能受体的信号类型。该研究计划的第一个目标是详细研究β2-肾上腺素能受体如何向T淋巴细胞发送信号。该计划的第二个目标是确定儿茶酚胺如何影响T淋巴细胞的功能，即它们与免疫相关的扩张和效应功能。*意义：适应性免疫反应对于对抗感染是必要的，但也可能导致自身免疫，即一个人自己的器官受到免疫系统的攻击。自身免疫性疾病影响着数以百万计的加拿大人，尤其是女性。与儿茶酚胺的联系表明，压力(慢性或其他)会影响适应性免疫。我们将取得的预期结果将增加我们对免疫系统的基本了解，并帮助科学家和医生更好地治疗感染和自身免疫。这项工作也适用于维持牲畜和鱼类的健康免疫力。******